Phosphate Buffer Solution Control Group Research Articles

Mechanism of maggot debridement therapy in promoting wound angiogenesis in patients with diabetic foot ulcer

Mechanism of maggot debridement therapy in promoting wound angiogenesis in patients with diabetic foot ulcer

Study on mechanisms of interleukin-17A regulating the expressions of interleukin-1β and interleukin-23 in mouse keratinocytes

Objective: To investigate the mechanisms of interleukin-17A (IL-17A) regulating the expressions of IL-1β and IL-23 in mouse keratinocytes (KCs). Methods: Primary KCs were isolated from the skin of 400 newborn male and female wild type C57BL/6 mice and cultured in 24-well plates with Roswell Park Memorial Institute 1640 medium containing fetal bovine serum in the volume fraction of 10% for the following experiments. (1) The cells were divided into phosphate buffer solution (PBS) control group and IL-17A stimulation group according to the random number table (the same grouping method below), which were cultured with 10 μL PBS or 10 μL IL-17A in the mass concentration of 100 ng/mL for 6 hours, respectively. The expression levels of IL-1β and IL-23 mRNA in cells were detected by real-time fluorescence quantitative reverse transcription polymerase chain reaction (RT-PCR), with 3 samples in each group. (2) The cells were divided into dimethyl sulfoxide (DMSO) control group, IL-17A+ DMSO group, IL-17A+ nuclear factor κB (NF-κB) inhibitor group, IL-17A+ signal transduction and activator of transcription 3 (STAT3) inhibitor group, IL-17A+ extracellular signal-regulated kinase 1 (ERK1) inhibitor group, IL-17A+ ERK2 inhibitor group, and IL-17A+ c-Jun N-terminal kinase (JNK) inhibitor group. The reagents were added to cells in corresponding groups respectively and cultured for 6 hours. The volume of each reagent was 10 μL, the mass concentration of IL-17A was 100 ng/mL, and the molarity concentrations of NF-κB, STAT3, ERK1, ERK2, JNK signal pathway inhibitors PDTC, S3I-201, SCH772984, SCH772984, SP600125 were 5 μmol/L, 100 μmol/L, 4 nmol/L, 1 nmol/L, and 10 μmol/L, respectively. The expression levels of IL-1β mRNA and IL-23 mRNA in cells were detected by real-time fluorescence quantitative RT-PCR, with 3 samples in each group. (3) The cells were grouped and treated the same as those in experiment (1). The levels of NF-κB phosphorylation, STAT3 phosphorylation, ERK phosphorylation, and JNK phosphorylation were detected by Western blotting, with 3 samples in each group. Data were statistically analyzed with two-tailed Student t test, one-way analysis of variance, t test, and Bonferroni correction. Results: (1) After culture of 6 hours, compared with those in PBS control group, the expression levels of IL-1β and IL-23 mRNA in cells in IL-17A stimulation group were significantly increased (t=13.46, 6.72, P<0.01). (2) After culture of 6 hours, the expression levels of IL-1β and IL-23 mRNA in cells in DMSO control group, IL-17A+ DMSO group, IL-17A+ NF-κB inhibitor group, IL-17A+ STAT3 inhibitor group, IL-17A+ ERK1 inhibitor group, IL-17A+ ERK2 inhibitor group, and IL-17A+ JNK inhibitor group were 1.00±0.11, 4.01±0.32, 0.32±0.06, 1.76±0.43, 3.62±0.24, 3.80±0.43, 4.26±0.74 and 1.03±0.29, 4.08±0.34, 4.76±0.38, 4.70±0.21, 1.06±0.42, 0.92±0.21, 0.39±0.05, respectively. Compared with those in DMSO control group, the expression levels of IL-1β and IL-23 mRNA in cells in IL-17A+ DMSO group were significantly increased (t=9.24, 12.60, P<0.01). Compared with that in IL-17A+ DMSO group, the expression level of IL-1β mRNA was significantly decreased in cells in IL-17A+ NF-κB inhibitor group and IL-17A+ STAT3 inhibitor group (t=11.34, 6.91, P<0.01). Compared with that in IL-17A+ DMSO group, the expression level of IL-23 mRNA was significantly decreased in cells in IL-17A+ ERK1 inhibitor group, IL-17A+ ERK2 inhibitor group, and IL-17A+ JNK inhibitor group (t=12.44, 13.03, 15.21, P<0.01). (3) After culture of 6 hours, compared with those in PBS control group, the levels of NF-κB phosphorylation, STAT3 phosphorylation, ERK phosphorylation, and JNK phosphorylation in cells in IL-17A stimulation group were significantly increased. Conclusions: IL-17A promotes the transcription of IL-1β in mouse KCs through the phosphorylation of NF-κB and STAT3 pathways and IL-23 through the phosphorylation of ERK and JNK pathways.

Effects and mechanism of interleukin-17-modified mouse bone marrow mesenchymal stem cells on rejection reaction of allogeneic skin transplantation in mice

Effects and mechanism of interleukin-17-modified mouse bone marrow mesenchymal stem cells on rejection reaction of allogeneic skin transplantation in mice

Improved method for inducing chronic atrophic gastritis in mice.

BACKGROUNDChronic atrophic gastritis (CAG) is a common disease of the digestive system with pathological characteristics of a decreasing number, or disappearance, of inherent glands of the gastric mucosa. CAG has been defined as a precancerous condition of gastric cancer. Intestinal metaplasia or intraepithelial neoplasia accompanying atrophied glands of the stomach is regarded as one of the most important precancerous lesions of gastric cancer. As a common malignant tumour, gastric cancer remains without a satisfactory therapy and its pathogenesis remains unclear, seriously threatening human life. Therefore, some scholars have proposed to prevent the incidence of gastric cancer by avoiding precancerous lesions. If CAG can be reversed, the incidence of gastric cancer can be substantially reduced. To reverse and prevent CAG and study its pathogenesis and therapy, it is necessary to develop an ideal, safe, stable, animal model.AIMTo study a rapid, stable, and safe method of establishing a mouse model of human CAG.METHODSSix-week-old Kunming mice were divided into a phosphate buffered solution control group, a Helicobacter pylori (H. pylori) group, an N-methyl-N'-nitroguanidine (MNNG) group, an ammonia water group, and a group combining H. pylori, MNNG, and ammonia water (hereinafter referred to as the combined group). The mice were administrated with drinking water containing ammonia or infected with H. pylori through gavage. At the 30th, 60th, 90th, and 120th day after the last H. pylori infection, mice were selected randomly to collect their gastric mucosa for hematoxylin eosin staining, terminal nick-end labelling staining detection, and immunohistochemical staining for Bax and Bcl-2. In addition, H. pylori was isolated, cultured, and identified, and its extent of colonisation calculated. Blood was collected to detect inflammatory factors interleukin (IL)-1β, IL-8, and tumor necrosis factor (TNF)-α and immune function markers CD4 and CD8 to confirm successful establishment of the CAG model.RESULTSThe combined group showed slight CAG at the 90th day and moderate CAG at the 120th day, while other groups did not show CAG at that time.CONCLUSIONThe combination of H. pylori, MNNG, and ammonia is an effective method of developing a mouse model of human CAG.

MicroRNA-155 reduces inflammatory response induced by lipopolysaccharide in alveolar macrophages

To observe the effect of microRNA-155 (miR-155) on the inflammatory response of rat alveolar macrophages induced by lipopolysaccharide (LPS). The alveolar macrophages NR8383 of rat were cultured in vitro, the macrophages in logarithmic growth phase were harvested to conduct experiment. (1) The 1 mg/L LPS was used to stimulate the rat alveolar macrophages for 3, 6, 12, and 24 hours, a phosphate buffer solution (PBS) control group was also set up. Enzyme linked immunosorbent assay (ELISA) was used to detect the dynamic changes of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in the supernatant, and real-time quantitative reverse transcription-polymerase chain reaction (RT-qPCR) was used to detect the dynamics expression of miR-155 in the cells, which confirmed the optimal time for LPS stimulation was 12 hours. (2) Carboxyfluorescein (FAM) labeled mimic (FAM mimic) and inhibitor (FAM inhibitor) were used to transfect the alveolar macrophage, and the transfection effect was observed under inverted fluorescence microscope 6 hours later to confirm the optimal transfection concentration of mimic was 20 nmol/L, and the optimal transfection concentration of inhibitor was 100 nmol/L. miR-155 mimic and miR-155 inhibitor were transfected to alveolar macrophages respectively at the optimal transfection concentration for 24 hours, and 1 mg/L LPS was used to stimulate the cells for 12 hours. A mimic negative control + LPS group and an inhibitor negative control + LPS group were set up. The expressions of IL-1β and TNF-α in the supernatant were determined by ELISA to observe the regulation of miR-155 on inflammatory response of alveolar macrophages. (1) After stimulation of 1 mg/L LPS on alveolar macrophages, the contents of IL-1β and TNF-α in the supernatant and the expression of miR-155 in the cells were increased gradually with time prolongation, IL-1β and TNF-α contents peaked at 12 hours, and the expression of miR-155 peaked at 24 hours [as compared with PBS control group, IL-1β (ng/L): 910.43±36.09 vs. 22.66±7.84, TNF-α (ng/L): 3 138.39±394.10 vs. 233.92±8.84, miR-155 (2-ΔΔCt): 7.82±0.30 vs. 1, all P < 0.05]. (2) Under inverted fluorescence microscope, after 20 nmol/L FAM mimic or 100 nmol/L FAM inhibitor transfected alveolar macrophages for 6 hours, a large number of cells showed green fluorescence, indicating that the transfection was successful. The expression of miR-155 in the cells transfected with 20 nmol/L miR-155 mimic was up-regulated by (236.73±46.49) times as much as that in the negative control group (P < 0.05), and the levels of IL-1β and TNF-α in the supernatant of the cells stimulated by 1 mg/L LPS for 12 hours were significantly lower than those in the negative control group [IL-1β (ng/L): 324.37±36.59 vs. 799.31±39.44, TNF-α (ng/L): 1 554.01±342.48 vs. 3 020.49±418.30, both P < 0.05]. The miR-155 activity was significantly inhibited in the cells transfected with 100 nmol/L miR-155 inhibitor, and the expression of miR-155 was decreased by (4.00±3.26)% as compared with the negative control group, but the difference was not statistically significant (P > 0.05), and the levels of IL-1β and TNF-α in the supernatant of the cells stimulated by 1 mg/L LPS for 12 hours were significantly higher than those in the negative control group [IL-1β (ng/L): 1 358.98±212.04 vs. 878.68±53.42, TNF-α (ng/L): 4 225.57±281.11 vs. 2 881.32±286.08, both P < 0.05]. In LPS induced inflammatory response of alveolar macrophages, miR-155 plays an obvious inhibitory role.

Acquisition and the immunogenicity of the outer membrane FomA protein of Fusobacterium nucleatum

Objective: To express and purify outer membrane protein FomA of Fusobacterium nucleatum (Fn) through gene recombination technique with Escherichia coli (Ec) expression system, and to detect the immunogenicity and the immune effects of the recombinant protein on gingival tissues. Methods: The gene recombination technique and Ec expression system were used to express and purified the FomA protein. Totally 20 C57 mice were immuned with the protein or the phosphate buffer solution (PBS) buffer by subcutaneous injection (each 10 mice), and the specific FomA antibody was detection in mice serum. The immunogenicity of FomA protein was assessed by comparing the differences between groups. Furthermore, the model of mice gum abscess was constructed with Fn or Fn and Porphyromonas gingivalis (Pg) mixed suspension used the above mice. The score of the gingival abscess was recorded and the interleukin (IL)-1β in gum tissue and mice serum was determined by enzyme-linked immunosorbent assay method, and the differences of the indexes between groups were compared to evaluate the effect of the FomA protein immunization. Results: Totally 1.0-1.5 g FomA protein were successfully obtained and the protein purity was over 90%. The FomA specific antibody was detected in the serum of mice by subcutaneous injection of the protein, and the antibody titer reached the highest level in 2 weeks after secondary immunization. The model of submaxillary gingival abscess was successfully constructed. In the Fn model, the score of the FomA protein immune group was (1.82±0.35), and the PBS control group was (2.62±0.71), with statistically significant difference between the two groups (P=0.049). In the Fn+Pg mixture model, the score of gingival abscess in the FomA immune group (2.31±0.55) was lower than that in PBS group (3.63±0.45), and the difference was statistically significant (P=0.003). Both in Fn and Fn+Pg injection group, the concentration of IL-1β in the serum of FomA immune mice and gingival tissues was lower than that of PBS control mice (P<0.001). Conclusions: The recombinant FomA protein can be acquired by Ec expression system, and it can produce a certain level antibodies in the mice serum. The way of mice subcutaneously injected with the recombinant FomA protein can reduce the severity of periodontal infections caused by Fn and Pg.

Effect of Biomineralization Ability on Push-out Strength of Proroot Mineral Trioxide Aggregate, Mineral Trioxide Aggregate Branco, and Calcium Phosphate Cement on Dentin: An In vitro Evaluation.

Context:Biomineralization is a process which leads to the formation of an interfacial layer with tag-like structures at the cement-dentin interface. It is due to interaction of mineral trioxide aggregate (MTA) and Portland cement with dentin in phosphate-buffered solution (PBS). This study is aimed to evaluate the effect of influence of biomineralization process on push-out bond strength of ProRoot MTA (Dentsply Tulsa Dental, Tulsa, OK, USA), MTA Branco (Angelus Soluc¸o˜es Odontolo´gicas, Londrina, PR, Brazil) and calcium phosphate cement (BioGraft CPC).Aim:The aim of this study was to evaluate the effect of biomineralization process on the push-out strength of ProRoot MTA, MTA Branco, and CPC after mixing with 0.2% chlorhexidine gluconate solution (0.2% CHX) and 2% lidocaine solution (2% LA) on the bond strength of MTA-dentin.Materials and Methods:Dentin discs with uniform cavities were restored with ProRoot MTA, MTA Branco, and calcium phosphate cement after mixing with 0.2% CHX solution and 2% lidocaine solution. The samples were uniformly distributed into two groups. Experimental group being immersed in PBS solution and control group being immersed in saline for 2 months. Instron testing machine (Model 4444; Instron Corp., Canton, MA, USA) was used to determine the bond strength.Statistical Analysis Used:A two-way analysis of variance and post hoc analysis by Bonferroni test.Results:All samples immersed in experimental group displayed a significantly greater resistance to displacement than that observed for the samples in control group (P < 0.05). MTAs displayed a significantly greater resistance to displacement than calcium phosphate cements.Conclusion:The main conclusion of this study was that the push-out bond strength of the cements, mainly the MTA groups, was positively influenced by the biomineralization process.

Novel Approach for Evaluation of Bacteroides fragilis Protective Role against Bartonella henselae Liver Damage in Immunocompromised Murine Model

Bartonella henselae is a gram-negative facultative intracellular bacterium and is the causative agent of cat-scratch disease. Our previous data have established that Bacteroides fragilis colonization is able to prevent B. henselae damages through the polysaccharide A (PSA) in an experimental murine model. In order to determine whether the PSA is essential for the protection against pathogenic effects of B. henselae in immunocompromised hosts, SCID mice were co-infected with B. fragilis wild type or its mutant B. fragilis ΔPSA and the effects of infection on murine tissues have been observed by High-Frequency Ultrasound (HFUS), histopathological examination, and Transmission Electron Microscopy (TEM). For the first time, echostructure, hepatic lobes length, vascular alterations, and indirect signs of hepatic dysfunctions, routinely used as signs of disease in humans, have been analyzed in an immunocompromised murine model. Our findings showed echostructural alterations in all infected mice compared with the Phosphate Buffer Solution (PBS) control group; further, those infected with B. henselae and co-infected with B. henselae/B. fragilis ΔPSA presented the major echostructural alterations. Half of the mice infected with B. henselae and all those co-infected with B. henselae/B. fragilis ΔPSA have showed an altered hepatic echogenicity compared with the renal cortex. The echogenicity score of co-infected mice with B. henselae/B. fragilis ΔPSA differed significantly compared with the PBS control group (p < 0.05). Moreover the inflammation score of the histopathological evaluation was fairly concordant with ultrasound findings. Ultrastructural analysis performed by TEM revealed no significant alterations in liver samples of SCID mice infected with B. fragilis wild type while those infected with B. fragilis ΔPSA showed the presence of collagen around the main vessels compared with the PBS control group. The liver samples of mice infected with B. henselae showed macro-areas rich in collagen, stellate cells, and histiocytic cells. Interestingly, our data demonstrated that immunocompromised SCID mice infected with B. henselae and co-infected with B. henselae/B. fragilis ΔPSA showed the most severe morpho-structural liver damage. In addition, these results suggests that the HFUS together with histopathological evaluation could be considered good imaging approach to evaluate hepatic alterations.

Investigation of the sensitivities of two different serotypes of Streptococcus pneumoniae in C57BL/6 mice with acute otitis media

To compare the sensitivities of two different serotypes of Streptococcus pneumoniae in acute otitis media of C57BL/6 mice. The middle ear cavity of C57BL/6 mice were inoculated via intratympanic injection of Streptococcus pneumoniae TIGR4 or 6B 1×10(8) CFU, and the control group were inoculated equivalent phosphate buffered solution (PBS). The incidence of mice, development of otitis media and the middle ear lavage fluid pathological changes by HE staining, as well as cell counts and cytokine levels were investigated. After inoculated with Streptococcus pneumoniae TIGR4, 6B and PBS, the survival rate of 6B group was significantly less than TIGR4 group and PBS control group (P < 0.01). Inflammatory cells in the middle ear cavity were mainly neutrophils, and the inflammatory cells recruitment in TIGR4 group were more than 6B group; The levels of IL-6 and TNF-α in the middle ear lavage fluid in TIGR4 group and 6B group were significantly increased compared with PBS control group, while the TIGR4 group were significantly increased compared with 6B group;6B group had delayed bacterial clearance in the middle ear. The study implied that Streptococcus pneumoniae 6B had higher pathogenicity for acute otitis media in C57BL/6 mice than TIGR4.

The effects of celecoxib-poly lactide-co-glycolide microparticles on rat retina after intravitreai injection

Objective To investigate the effects of （CEL-PLGA MS） on rat retina after intravitreal injection. celecoxib-poly lactide-co-glycolide microparticles Methods A total of 32 male Brown Norway rats were randomly divided into CEL-PLGA-MS group and celecoxib group, 16 rats in each group. The rats in CEL-PLGA-MS group were divided into four dosage group, four rats in each group, which received intravitreal injection of PLGA with celecoxib at the concentration of 40, 80, 160, 320μmol/L, respectively. The rats in celecoxib group were divided into four dosage group, four rats in each group, which receivedintravitreal injection of celecoxib at the concentration of 40, 80, 160, 320 μmol/L, respectively. Phosphate buffer solution （PBS） was injected in two rats as PBS control group. Two rats as normal control group received no treatment. The difference of retinal thickness among groups was measured by optical coherence tomography （OCT）. The morphological and histological change of retina was evaluated under light microscope and transmission electron microscope. Results There was no difference of retinal thickness between normal control group and PBS control group （F = 0.12, P~〉 0.05）. At the first week after injection, the retinal thickness of CEL-PLGA-MS group and celecoxib group were thicker than that in normal control group and PBS control group （F = 9.62, 46.13; P〈 0.01）. The retinal thickness of celecoxib group was thicker than that in CEL-PLGA-MS group （F = 165.15, P〈 0.01）. The retinal thickness was estimated equal among 40, 80, 320 μmol/L dosage groups in CEL-PLGA MS group （F= 4.79, P~0.01）. The retinal thickness of 160, 320 μmol/L dosage group were thicker than that in 40, 80 μmol/L dosage group in celecoxib group （F=28.10, P〉0.01）. At the second week after injection, there was no difference of retinal thickness between CEL-PLGA-MS and celecoxib group （F= 3.79, P〈0. 05） ; the retinal thickness of CEL-PLGA-MS and celecoxib group became thinner gradually compare to the first week after injection （F=7.28, 103.99; P〈0.01）. At the fourth week after injection, the retinal thickness of celecoxib group was thicker than that in CEL-PLGA-MS group （F= 19. 11, P〈0. 01）. The retinal thickness of CEL-PLGA-MS group was approximately the same to normal control group and PBS control group （F=2.02, P〉0.05）. The retinal thickness of celecoxib group was thicker than that in normal control group and PBS control group. No considerable abnormality of the retina was seen by light microscope and the retinal thickness corresponded with the values measured by OCT at the first week after injection. The abnormal structures of the retina were seen in 160, 320 μmol/L dosage group of celecoxib group and inner changed evidently by the transmission electron microscope. Disordered arrangement of microfilaments, dilated microtubule and some mitoehondria vacuolation were observed in 320 μmol/L dosage group of celecoxib group. Others changed slightly. Conclusions CEL-PLGA-MS has less toxicity on the retina than free-celecoxib after intravitreal injection. The safety of intravitreal injection with CEL-PLGA-MS is better than celecoxib. Key words: Cyclooxygenase 2 inhibitors/toxicity; Cyclooxygenase 2 inhibitors/diagnostic use; Delayed-action preparations/toxicity; Choroidal neovascularization/drug therapy

Recombined adenovirus of p21 inhibit the proliferation of Rhesus retinal vascular endothelial cells in vitro

Objective To observe the inhibitory effect of recombined adenovirus of p21 (rAd-p21) on the proliferation of Rhesus retinal vascular endothelial cell line (RF/6A). MethodsRF/6A cells were cultured in vitro which divided into phosphate buffered solution (PBS) group, rAd-p21 transfection group and negative control (NC) group. Plasmid vectors were transfected into RF/6A cells. The expression of p21mRNA and protein in RF/6A cells were measured by RT-PCR and Western blot respectively. The cell cycle distribution was analyzed by flow cytometry. Endothelial-cell tube formation assay was performed in Matrigel. Results The expression of p21 mRNA and protein in rAd-p21 transfection group were higher than that in PBS and negative control group. The cell cycle distribution showed that the proportion of G0/G1 cells in rAd-p21 transfection group[(67.45 ± 11.61) ％]was apparently higher than that in the negative control group[(41.55±8.99)％]and PBS group[(40. 76±6.66) ％](F=21.284, P =0. 000 ). The number of endothelial-cell tubes in the rAd-p21 transfection group (3.86±1.21) was apparently less than that in the negative control group (7.62±2.69) and PBS group (8.25±3.19) (F=7.138,P=0.004).Conclusions The p21 mRNA and protein can stably express in RF/6A cells after rAd-p21 transfection.RAd-p21 can inhibit the proliferation of RF/6A cells. Key words: Retinal neovascularization/ prevention & control; Gene transfer techniques; Transfection; Animal experimentation

Up-regulation interleukin-6 and interleukin-8 by activated protein C in lipopolysaccharide-treated human umbilical vein endothelial cells

To investigate the effect of activated protein C (APC) on inflammatory responses in human umbilical vein endothelial cells (HUVEC) stimulated with lipopolysaccharide (LPS). The second passage of collagenase digested HUVEC was divided into the following groups: serum free medium control group (SFM control), phosphate buffer solution control group (PBS control), LPS group with final concentration of 1 microg/ml (LPS group), APC group with final concentration of 7 microg/ml, Pre-APC group (APC pretreatment for 30 min prior to LPS challenge), and Post-APC group (APC administration 30 min after LPS challenge). Supernatant was harvested at 0, 4, 8, 12 and 24 h after LPS challenge. Interleukin-6 (IL-6) and Interleukin-8 (IL-8) levels were analyzed with ELISA. Cells were harvested at 24 h after LPS challenge, and total RNA was extracted. Messenger RNA levels for IL-6 and IL-8 were semi-quantitatively determined by RT-PCR. Compared with control group, IL-6 and IL-8 levels steadily increased 4 to 24 h after LPS stimulation. APC treatment could increase LPS-induced IL-6 and IL-8 production. The mRNA levels of IL-6 and IL-8 exhibited a similar change. APC can further increase the level of IL-6 and IL-8 induced by LPS. The effect of these elevated cytokines is still under investigation.

Topical and Subcutaneous ??-Interferon Fails to Suppress Corneal Neovascularization

Corneal neovascularization is a potentially blinding complication of a variety of corneal disorders. alpha-Interferon has been shown to inhibit endothelial cell migration and proliferation. It has been used successfully in the treatment of pediatric pulmonary hemangioma and hairy cell leukemia. This study was undertaken to evaluate the effect of topical and subcutaneous (s.c.) alpha-interferon on corneal neovascularization. Corneal neovascularization was induced in 40 male New Zealand white rabbits by placing silk sutures (7.0) bilaterally in each rabbit eye at the 3 and 9 o'clock positions of the cornea, 3 mm from the limbus. Animals were randomized into two main treatment groups for topical (group 1) and s.c. (group 2) administration of interferon. Group 1 (n = 24) was then randomized into four subgroups and treated daily with topical doses of (a) rabbit specific alpha-interferon; (b) alpha-interferon plus 1% prednisolone acetate; (c) 1% prednisolone acetate; and (d) buffered phosphate control. Group 2 (n = 16) was randomized into two subgroups that received s.c. injections every other day of (a) alpha-interferon and (b) phosphate buffer. Rate of corneal neovascularization was documented photographically, with the end-point being the arrival of vessels at the suture for each group. The results of this study indicated that at the concentration and dosing regimens we used, neither topical nor s.c. alpha-interferon inhibits the rate of corneal vascular growth significantly when compared with our phosphate buffered solution control group (p = 0.88 and p = 0.84, respectively). Prednisolone acetate appeared to be the most effective in inhibiting corneal neovascularization (p = 0.003).(ABSTRACT TRUNCATED AT 250 WORDS)